Positive pressure therapies include nasal continuous positive airway pressure (CPAP) as used in the treatment of obstructive sleep apnea (OSA) and nasal intermittent positive pressure ventilation for breathing support in chronic restrictive and obstructive lung diseases and associated acute exacerbations. A user will wear a nasal or nose mouth mask connected by a tube or flexible conduit connected to a positive pressure air flow generator. The mask system consists of a flexible mask cushion, which also acts as a gasket to prevent loss of gas pressure inside the mask, attached to a mask frame or manifold and attached to the user's head via a head strap or head gear. The mask assembly usually covers the nose but can also cover both the nose and mouth to circumvent mouth leaks and breathing. Alternatively, the mask device may be designed to sit superficially on or be partially inserted into the user's nares.
The general purpose of the apparatus consisting tubing, mask and pressure generator or source is to maintain a positive gas pressure, typically between 0 and 40 centimeters of water (cm H2O), but most practically between 4 and 20 cm H2O, within the user's airway to improve or facilitate gas exchange within the gas exchanging areas of the lung and/or prevent collapse of the upper or non-exchanging parts of the upper airway. Most commonly a single pressure (CPAP) will be used to treat sleep apnea, while 2 pressures can be used to expand and deflate the lungs where ventilatory support is required in cases of respiratory insufficiency. This technique may also have a role to improve comfort in treatment of sleep apnea.
Treatment of OSA, using positive pressure techniques, is often prescribed using fixed CPAP, with the pressure preset in a sleep laboratory. Alternatively, an automatic machine may be used with an ability to provide CPAP where pressure is continuously, gradually and automatically adjusted during a treatment session in response to upper respiratory air flow characteristics, such as the shape of the inspiratory flow time curve; presence of snore or associated pressure and flow changes or overt apnea. Once established, treatment is routinely used in the home.
Alternatively a separate pressure may be applied during inspiration and a lower pressure used for expiration such as described in U.S. Pat. No. 5,148,802. In this case the pressures will be preset and the transition from one pressure to another will be initiated by the patient as they move through inspiration to expiration and vice versa. The rational for this modality is that the patient will find the exhalation pressure lower and hence more comfortable to breathe against, particularly in sleep apnea. In addition the device augments ventilation in addition to providing positive pressure by assisting with movement of air into and out of the lungs by successive pressure inflation and deflation. This will be useful where the patient has some lung insufficiency or muscular deficiency either in combination with or absence of upper airway instability.
Currently automatic selection of pressures for this bi-level modality is limited or difficult particularly during sleep where ventilatory support for hypoventilation syndromes (or hyperventilation/hypoventilation syndromes such as Cheyne Stokes Respiration) and sleep apnea must be managed simultaneously (complex sleep apnea); in sleep apnea the expiratory pressure needed to negate airway closure at the immediate transition from the expiratory pause to inspiration must be set in conjunction with ventilatory support parameters. In automatically controlled CPAP, that is having expiratory and inspiratory pressures set equally, it is possible to set this pressure by simply monitoring inspiratory flow behaviour as discussed above. Typically the 2 pressures will be established manually in a controlled study wherein the user is monitored and the pressures adjusted to achieve the desired treatment outcomes which can include control of sleep apnea as well maintaining ventilatory requirements
A further method of support for providing respiratory assistance in respiratory impairment is described in U.S. Pat. No. 4,773,411. In this technique, termed airway pressure release ventilation (APRV), support is provided substantially by CPAP to enhance residual functional capacity with periodic release of pressure to provide passive reduction of lung volume. This periodic release is not breath to breath and the user will typically breathe spontaneously at the preset CPAP pressure. Settings are manually selected by attendants, that is the CPAP level, the release level and release duration as well the number of breaths depending on the patient's respiratory state and hence is suited to attended or in hospital situations and is not designed for treating simple or complex sleep apnea.
During quiet breathing without pressure assistance, such as during sleep or awake involuntary, or spontaneous, breathing, there is a pronounced period of respiratory quiescence whereby the elastic recoil of the lungs and chest wall returns the lungs to their functional residual capacity (FRC). In response to chemoreceptor activity the diaphragmatic muscles, principally, will be innervated to increase negative intrapleural pressure thereby expanding the lung volume. Normally this activity is under autonomic control but during the awake state it may be overridden and air may be moved consciously into and out of the lungs by diaphragmatic and intercostal muscles. In this sense respiration is distinguished from other life sustaining functions, such as heart rate, cardiac contractility and pressure which are entirely within the control of the autonomic system and the individual only has indirect control over these parameters.
Respiratory rate and duration is under control of the respiratory centre located in the reticular substance of the medulla oblongata and pons. These centres respond to changes in blood gas levels and acidity either directly or indirectly through peripheral chemoreceptors. Functionally it may be divided into three neuronal groups comprising the dorsally located inspiratory area, ventrally located expiratory area and the pneumotaxic area of the pons. Normally the rhythmic nature of breathing is controlled principally by the inspiratory area. Neurones in this area are able to oscillate spontaneously in a crescendo like manner gradually increasing intensity causing the diaphragm to contract and causing an inspiratory movement. This gradual increase lasts about 2 seconds in quiet breathing. Conversely during expiration, the inspiratory area becomes dormant for about 3 seconds and the cycle repeats. During normal quiet breathing the expiratory area remains substantially dormant as exhalation is possible through elastic recoil of the lung and chest wall, although some muscular innervation may be present to control smoothness of expiration to prevent expiratory heave, such as seen during sighs and other involuntary movements to for example rebalance atelectic regions in the lungs.
During nasal CPAP therapy, for treatment of sleep apnea for example, we have 2 important observations. First the lungs are expanded by an amount proportional to the compliance of the lungs and chest wall and the applied air pressure. Hence, the FRC is increased over that observed when the user is breathing at atmospheric pressure. This can be described by the followingFRC(CPAP)=FRC atm+ΔVCPAP  (1)
Where FRC (CPAP)=functional residual capacity on CPAP
FRC atm=functional residual capacity at atmospheric pressure
ΔVCPCP=change in lung volume after CPAP is applied
Normal compliance for lungs and chest wall is about 0.13 liters/cm H20. Hence at 10 cm H2O this delta volume is in the vicinity of 1.3 liters. This figure may be reduced for restrictive diseases, however most sleep apnea patients and those with obstructive pulmonary diseases will have normal or near normal lung and thoracic compliance. To place this in perspective, tidal volume during quiet breathing is about 500 ml. Hence we can see that CPAP at therapeutic levels distends the lungs by more the twice the tidal volume, and will reduce the inspiratory reserve volume.
Second, CPAP for many users, as seen for example in those receiving treatment for sleep apnea, feels unnatural and in some uncomfortable. This is often described as discomfort of having to breathe out against the CPAP pressure. For this reason, an alternative to CPAP is to provide a lower pressure during expiration, so called bi-level treatment as discussed. The problem with this modality is that it is not simple to automatically determine the optimal minimum or expiratory pressure level needed to prevent airway closure at the transition from expiration to inspiration if user initiated.
Based on these observations it is possible to postulate that during quiet breathing on CPAP, the breathing cycle is reversed or partly reversed. That is inspiratory cycle occurs to a varying degree by positive pressure inflation/recoil and expiration by innervation of expiratory muscles as opposed to elastic recoil.
In this case equation 1 may be more appropriately written as equation 2IRV(CPAP)=TLC−(FRC atm+ΔVCPAP)  (2)
Where
TLC=total lung capacity
IRV=inspiratory reserve volume
CPAP=applied pressure which limits inspiratory drive for quiet breathing.
Since expiration, in the absence of CPAP, is by passive recoil in quiet breathing, this may explain some of the discomfort during routine CPAP, for example, that is expiration now requires active muscular effort. Another factor may be the continuous expansion of the lungs and chest wall by CPAP. This observation, however, is complicated by virtue of the fact that respiration can be overridden by voluntary effort. The unnatural sensation of CPAP during consciousness may lead to an “abnormal” voluntary or cortical response. However, if we assume that involuntary exhalation during CPAP use occurs against pressure recoil, this would then suggest that the medullary inspiratory area can be down regulated to interplay with the expiratory centre to maintain background respiratory rate (however respiratory control is further complicated by the pneumotaxic centre located in the pons which acts to either inhibit or uninhibit the inspiratory centre). A further explanation is related to stretch receptors within the walls of the bronchi and bronchioles which if over stretched, as may be seen during CPAP therapy, further limit inspiratory effort particularly during involuntary quiet breathing and sleep. This is known as the Hering-Breuer reflex and is known to become important once the lung volume is increased by about 1.5 liters above FRC; this would appear to be consistent with therapeutic CPAP levels.
However, CPAP treatment remains broadly crude and variably tolerated. While acceptable for most severely affected patients, more comfortable and physiologic solutions are seen as essential to ensure an otherwise effective therapy does not itself become self-limiting for a very debilitating and widespread condition. Furthermore, complex sleep apnea requires more complex solutions to provide background ventilatory support as well as sleep apnea treatment. Finally automatic selection of pressures simplifies prescription and remains adapative to a specific user's needs.